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神经生长因子增加氨甲酰胆碱诱导的22Na+流入嗜铬细胞瘤PC12h细胞的量。

Increase of carbamylcholine-induced 22Na+ influx into pheochromocytoma PC12h cells by nerve growth factor.

作者信息

Mitsuka M, Hatanaka H

出版信息

Brain Res. 1984 Feb;314(2):255-60. doi: 10.1016/0165-3806(84)90047-6.

DOI:10.1016/0165-3806(84)90047-6
PMID:6322934
Abstract

Carbamylcholine (CCh)-induced 22Na+ influx into clonal rat pheochromocytoma PC12h cells increased remarkably by culturing the cells in the presence of nerve growth factor (NGF) at a concentration of 50 ng/ml. After 2-4 days in culture with NGF, the CCh-induced 22Na+ influx into cells was enhanced 3- to 5-fold compared to the influx into NGF-untreated cells. No increase of CCh-induced 22Na+ influx was seen prior to 15 h. The ED50 value for NGF to increase the responsiveness was 4.6 ng/ml. This effect could not be mimicked by the addition of 1 mM dibutyryl cyclic AMP. Besides NGF, epidermal growth factor increased the CCh-induced 22Na+ influx into cells to a lower extent that NGF did. Insulin and dexamethasone had no effect. By contrast, the amount of [125I] alpha-bungarotoxin binding to PC12h cells was not changed when cultured in the presence of NGF. It is concluded that the functional nAChR and alpha-bungarotoxin binding sites of PC12h cells are controlled by different mechanisms.

摘要

在50 ng/ml神经生长因子(NGF)存在的情况下培养克隆大鼠嗜铬细胞瘤PC12h细胞,氨甲酰胆碱(CCh)诱导的22Na+流入细胞的量显著增加。在用NGF培养2 - 4天后,与未用NGF处理的细胞相比,CCh诱导的22Na+流入细胞的量增加了3至5倍。在15小时之前未观察到CCh诱导的22Na+流入增加。NGF增加反应性的半数有效剂量(ED50)值为4.6 ng/ml。添加1 mM二丁酰环化腺苷酸不能模拟这种效应。除了NGF外,表皮生长因子使CCh诱导的22Na+流入细胞的量增加的程度低于NGF。胰岛素和地塞米松没有作用。相比之下,在NGF存在的情况下培养时,与PC12h细胞结合的[125I]α-银环蛇毒素的量没有变化。得出的结论是,PC12h细胞的功能性烟碱型乙酰胆碱受体(nAChR)和α-银环蛇毒素结合位点受不同机制控制。

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Increase of carbamylcholine-induced 22Na+ influx into pheochromocytoma PC12h cells by nerve growth factor.神经生长因子增加氨甲酰胆碱诱导的22Na+流入嗜铬细胞瘤PC12h细胞的量。
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